Arterial Embolism Occurring During Systemic Heparin Therapy

Weismann, Rodger E.; Tobin, Richard W.

doi:10.1001/archsurg.1958.01280200041005

Cited by 282 publications

(120 citation statements)

References 4 publications

Supporting

Mentioning

108

Contrasting

Unclassified

Order By: Relevance

“…Three days after successful femoral embolectomy, and while continuing to receive heparin, she developed sudden occlusion of the distal aorta requiring distal aortic and bilateral iliac embolectomies. 3 Multiple thromboemboli were observed in 9 of the 10 patients reported. Six patients died as a result of the thromboembolism, and 2 survivors underwent above-knee amputation.…”

Section: Heparin-induced Arterial Embolismmentioning

confidence: 95%

“…This may explain why thrombocytopenia was not reported in the first 24 patients with heparin-induced arterial emboli. [3][4][5][6] In 1969, the term "heparin-induced thrombocytopenia" was used by Natelson 7 to describe a 78-year-old man with pulmonary embolism who developed severe thrombocytopenia after heparin. Over the ensuing days, 2 separate periods of heparin readministration were each characterized by abrupt platelet count declines and corresponding increases in fibrinogen.…”

mentioning

confidence: 99%

See 1 more Smart Citation

Heparin-induced thrombocytopenia: a historical perspective

Kelton

Warkentin

2008

Blood

169

113

View full text Add to dashboard Cite

Heparin was discovered 90 years ago, 1 and within 2 decades it was being widely used as an anticoagulant. 2 The numerous advantages of heparin lend to its broad use including its immediate onset of action, relatively short half-life (ϳ60 minutes), simple laboratory monitoring (aPTT), ability to be reversed (using protamine), and low cost. Despite a long experience of using heparin, the counterintuitive notion that an anticoagulant could be intensely prothrombotic took almost 4 decades to become recognized.Our understanding of heparin-induced thrombocytopenia (HIT) has increased considerably and to a large measure exemplifies the best of translational research. Sometimes, basic studies investigating the pathophysiology of HIT lead to clinical insights. In other instances, clinical observations prompted basic studies. Together, these basic and applied investigations have dramatically enhanced our understanding of the pathogenesis and treatment of HIT. Heparin-induced arterial embolismOn June 1, 1957, at the Fifth Scientific Meeting of the International Society of Angiology in New York, Rodger E. Weismann, an Assistant Professor of Clinical Surgery at the Dartmouth Medical School, and his Resident in Surgery, Dr Richard W. Tobin, described 10 patients who developed arterial embolism during systemic heparin therapy. 3 The first reported embolic event was a femoral artery embolic occlusion, which occurred in a 62-year-old woman who was receiving heparin because of a deep-vein thrombosis (DVT). Three days after successful femoral embolectomy, and while continuing to receive heparin, she developed sudden occlusion of the distal aorta requiring distal aortic and bilateral iliac embolectomies. 3 Multiple thromboemboli were observed in 9 of the 10 patients reported. Six patients died as a result of the thromboembolism, and 2 survivors underwent above-knee amputation. 3 The clots were described as "pale, soft, salmon-colored" and were composed mostly of fibrin, platelets, and leukocytes. The arterial emboli began on average 10 days after commencing heparin treatment.An additional 11 patients were described 5 years later by Roberts and colleagues. 4 These vascular surgeons noted the paradox of "unexplained arterial embolization [occurring] for the first time while being treated with heparin for some condition that could not of itself reasonably be expected to cause arterial emboli. All patients had been receiving heparin for 10 days or more when the initial embolus occurred." Thus, both groups 3,4 noted the temporal hallmark of HIT, a delay of approximately 1 week from initiation of heparin to onset of its thrombotic manifestations. Heparin-induced thrombocytopeniaRoutine platelet count measurements were not routinely performed until the 1970s. This may explain why thrombocytopenia was not reported in the first 24 patients with heparin-induced arterial emboli. [3][4][5][6] In 1969, the term "heparin-induced thrombocytopenia" was used by Natelson 7 to describe a 78-year-old man with pulmonary embolism who developed severe t...

show abstract

Section: Heparin-induced Arterial Embolismmentioning

confidence: 95%

mentioning

confidence: 99%

Heparin-induced thrombocytopenia: a historical perspective

Kelton

Warkentin

2008

Blood

169

113

View full text Add to dashboard Cite

show abstract

“…1 Development of thrombotic complications in patients given UFH treatment was first described in 1958. 2 The association between developing thrombocytopenia and occurrence of a thromboembolic event in patients being treated with UFH was reported at the start of the 1970s. 3 Later studies demonstrated that the incidence of heparin-induced thrombocytopenia (HIT) was lower than observed in previous studies and that was when it was recognized that heparin can cause reduced platelet counts via two mechanisms.…”

Section: Introductionmentioning

confidence: 99%

Trombocitopenia induzida por heparina em paciente com oclusão arterial aguda

et al. 2016

View full text Add to dashboard Cite

Heparin induced thrombocytopenia (HIT) is a serious complication of heparin anticoagulation and is associated with formation of anti-platelet factor 4. It usually occurs from the fifth day of treatment onwards, with a fall in platelet count of at least 50%. Venous or arterial thrombosis may occur as a result of concomitant platelet activation, with serious clinical repercussions. We present the case of a patient with antiphospholipid antibody syndrome who presented with acute arterial occlusion and was treated surgically and given unfractionated heparin intraoperatively and postoperatively. On the fifth day of anticoagulant treatment he exhibited a platelet count decreased by more than 50% compared to the count prior to heparin administration. The suspicion of heparin-induced thrombocytopenia and its diagnostic and therapeutic features are addressed in this therapeutic challenge paper.Keywords: thrombocytopenia; heparin; thrombophilia; diagnosis and therapy. ResumoA trombocitopenia induzida por heparina é uma complicação grave da terapêutica anticoagulante com heparina e está associada à formação de anticorpos antifator IV plaquetário. Costuma surgir a partir do quinto dia do tratamento, com queda de pelo menos 50% da contagem plaquetária. Em decorrência da ativação plaquetária concomitante, pode ocorrer quadro de trombose, venosa ou arterial, com repercussões clínicas graves. Apresentamos um caso de paciente portador de síndrome do anticorpo antifosfolípide, com quadro de oclusão arterial aguda, que foi tratado cirurgicamente e recebeu heparina não fracionada no intra e pós-operatório. No quinto dia de tratamento anticoagulante, apresentou queda maior de 50% da contagem de plaquetas em relação à contagem pré-heparina. A suspeita de trombocitopenia induzida por heparina e seus aspectos diagnósticos e terapêuticos serão abordados neste desafio terapêutico.

show abstract

“…Paradoxically, affected patients commonly present with thromboembolic phenomena [1][2][3][4]. Indeed, the frequent development of recurrent arterial and/or venous thrombosis in patients with heparin-induced thrombocytopenia (HIT) is almost unique among drug-induced immune platelet disorders.…”

Section: Introductionmentioning

confidence: 99%

“…idiotype). Upon stimulation with the autoantibody carrying a specific idiotype (Ab 1 ), naive mice develop anti-autoantibodies (anti-Id ¼ Ab 2 ), and after 1-2 months, anti-anti-autoantibodies (anti-anti-Id ¼ Ab 3 ) that may have similar binding specificities to Ab 1 . Coincident with expression of Ab 3 , immunized mice often develop an overt autoimmune condition that resembles the human disorder from which the inducing autoantibody (Ab 1 ) was obtained, e.g.…”

Section: Introductionmentioning

confidence: 99%

Pathogenicity of human anti-platelet factor 4 (PF4)/heparin in vivo: generation of mouse anti-PF4/heparin and induction of thrombocytopenia by heparin

Blank

Cines

Arepally

et al. 1997

Clinical and Experimental Immunology

View full text Add to dashboard Cite

SUMMARYHeparin-induced thrombocytopenia/thrombosis (HIT) is a severe thrombotic disorder that occurs in Ϸ1% of patients treated with heparin. Affected patients commonly develop antibodies that recognize PF4/heparin complexes that may form on the surface of activated platelets and on the endothelium. However, it has not been established that anti-PF4/heparin antibodies are responsible for the clinical manifestations of HIT. To address this issue, we employed a recently developed model of active immunity to study the effect of IgG anti-

show abstract

Arterial Embolism Occurring During Systemic Heparin Therapy

Cited by 282 publications

References 4 publications

Heparin-induced thrombocytopenia: a historical perspective

Heparin-induced thrombocytopenia: a historical perspective

Trombocitopenia induzida por heparina em paciente com oclusão arterial aguda

Pathogenicity of human anti-platelet factor 4 (PF4)/heparin in vivo: generation of mouse anti-PF4/heparin and induction of thrombocytopenia by heparin

Contact Info

Product

Resources

About